Evidence map›Paper›PMID 42477610›Full record

ArticleBMC neurology2026

Tyrosine kinase inhibitor-associated cerebral vasculopathy with a distinct non-enhancing vessel wall phenotype: a case report.

Jeong Eun Yang, Jae Ho Jeon, Young Rok Do, Jaeseob Yun

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In one paragraph

Article in BMC neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

4 authors.

Jeong Eun YangDepartment of Neurology, Dong-san Hospital, Keimyung University School of Medicine, Daegu, Korea.
Jae Ho JeonDepartment of Neurology, Dong-san Hospital, Keimyung University School of Medicine, Daegu, Korea.
Young Rok DoDepartment of Hematology and Oncology, Dong-san Hospital, Keimyung University School of Medicine, Daegu, Korea.
Jaeseob YunDepartment of Neurology, Dong-san Hospital, Keimyung University School of Medicine, Daegu, Korea. jaeseobyun89@gmail.com.ORCID https://orcid.org/0000-0002-8884-4114

Funding

Research grant from the Convergence Medical Institute, Pusan National University Hospital Project No. CMIT2026-04
6 · The paper itself

Abstract

backgroundTyrosine kinase inhibitors (TKIs) are associated with adverse vascular events, including cerebrovascular stenosis. However, most reported cases rely on luminal imaging, and the arterial wall characteristics of TKI-associated vasculopathy remain insufficiently characterized. CASE PRESENTATION: A 47-year-old man with chronic myeloid leukemia developed recurrent transient ischemic attacks during long-term exposure to multiple tyrosine kinase inhibitors, including sequential treatment with nilotinib and ponatinib. Neurovascular imaging revealed extensive multifocal steno-occlusive lesions involving both intracranial and extracranial arteries, accompanied by severe hemodynamic compromise. High-resolution vessel wall MRI demonstrated diffuse circumferential wall thickening with negative remodeling in both distal internal carotid arteries and eccentric thickening along the anterior walls of the bilateral M1 segments of the middle cerebral artery. Notably, no definite mural enhancement was observed. Following discontinuation of ponatinib and transition to alternative therapy, cerebral perfusion improved at two months, and the patient remained clinically stable without recurrent ischemic events.

conclusionsThis case illustrates a potentially distinct vessel wall thickening pattern in TKI-associated vasculopathy, providing information beyond luminal stenosis. The absence of definite mural enhancement and clinical and hemodynamic improvement after treatment modification suggest a drug-related vascular component. Vessel wall imaging may aid in the evaluation of this condition and inform management strategies.

Indexed as

Cerebrovascular DisordersImidazolesProtein Kinase InhibitorsPyridazinesHumansLeukemia, Myelogenous, Chronic, BCR-ABL PositiveMagnetic Resonance ImagingMaleMiddle AgedPhenotypePyrimidinesTyrosine Kinase InhibitorsImidazolesnilotinibponatinibProtein Kinase InhibitorsPyridazinesPyrimidinesTyrosine Kinase InhibitorsCase reportCerebrovascular diseaseIntracranial stenosisTyrosine kinase inhibitorVessel wall MRI

Identifiers

PMID42477610
PMCPMC13663275

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